The researchers found that the allele classes of the variable number of tandem repeats (VNTRs) upstream of INS promoter, the so-called type-1 diabetes (T1D) susceptibility locus 2, affected INS transcription, and suggested that higher amounts of thymic insulin could promote a more effective purge of the related self-reactive thymocyte clone (5–7). The gene discussed is INS; the disease is type 1 diabetes mellitus.